F Fontana

University of Bologna, Bolonia, Emilia-Romagna, Italy

Are you F Fontana?

Claim your profile

Publications (62)195.48 Total impact

  • [Show abstract] [Hide abstract]
    ABSTRACT: The occurrence of depression in patients with coronary heart disease (CHD) substantially increases the likelihood of a poorer cardiovascular prognosis. Although antidepressants are generally effective in decreasing depression, their use in patients with CHD is controversial. We carried out a meta-analysis to evaluate the health effects of selective serotonin reuptake inhibitors (SSRIs) versus placebo or no antidepressants in patients with CHD and depression. Observational studies and randomized controlled trials (RCTs) were searched in MEDLINE, EMBASE, PsycINFO, Cochrane Controlled Clinical Trial Register and other trial registries, and references of relevant articles. Primary outcomes were readmission for CHD (including myocardial infarction, unstable angina, and stroke) and all-cause mortality; the secondary outcome was severity of depression symptoms. Seven articles on 6 RCTs involving 2,461 participants were included. One study incorrectly randomized participants, and another was a reanalysis of RCT data. These were considered observational and analyzed separately. When only properly randomized trials were considered (n = 734 patients), patients on SSRIs showed no significant differences in mortality (risk ratio 0.39, 95% confidence interval 0.08 to 2.01) or CHD readmission rates (0.74, 0.44 to 1.23) compared to controls. Conversely, when all studies were included, SSRI use was associated with a significant decrease in CHD readmission (0.63, 0.46 to 0.86) and mortality rates (0.56, 0.35 to 0.88). A significantly greater improvement in depression symptoms was always apparent in patients on SSRIs with all selected indicators. In conclusion, in patients with CHD and depression, SSRI medication decreases depression symptoms and may improve CHD prognosis.
    The American journal of cardiology 01/2011; 107(7):972-9. · 3.58 Impact Factor
  • Source
    [Show abstract] [Hide abstract]
    ABSTRACT: We investigated the relationship between intima-media thickening (IMT) as an expression of preclinical atherosclerosis and coronary risk factors, including the autonomic nervous system and inflammation markers, in depressed subjects free from coronary artery disease. We studied 391 asymptomatic subjects with a cluster of risk factors, and we evaluated depression using the Beck Depression Inventory. IMT of the common carotid artery was determined by B-mode ultrasound imaging. Traditional risk factors for atherosclerosis were recorded. Markers of inflammation (C-reactive protein, CRP; interleukin 6, IL-6) and heart rate variability (time domain) were determined. A total of 90 (23.0%) subjects showed a depressive symptomatology. The average IMT was increased in depressed subjects (0.87+/-0.35 mm) at risk for CHD but free from disease as compared to controls (0.77+/-0.19 mm; p<0.001). Heart rate variability was reduced in depressed subjects. Levels of SDNN (103+/-14 ms) and SDANN (93+/-20 ms) were decreased in depressed subjects as compared to non-depressed subjects (SDNN 113+/-22 ms and SDANN 108+/-35 ms; p<0.001). Subjects with depression had higher CRP (1.14+/-0.65 mg/dl) and IL-6 (2.00+/-0.40 pg/ml) than subjects without depression (CRP: 0.79+/-0.34 mg/dl; IL-6: 1.6+/-0.6 pg/ml; p<0.001, respectively). In multivariate analysis, depression was positively correlated with CRP and IL-6 and IMT, and inversely associated with levels of SDANN. IMT is higher in depressed subjects, indicating that atherosclerosis is accelerated in this sub-group of patients. This is mainly due to patho-physiological mechanisms which connect depression and coronary artery disease, such as inflammation and imbalance of the autonomic nervous system.
    Atherosclerosis 09/2010; 212(1):292-8. · 3.71 Impact Factor
  • [Show abstract] [Hide abstract]
    ABSTRACT: In vitro and in vivo studies demonstrated that nociceptin/orphanin FQ inhibits norepinephrine release, while the effects of norepinephrine on nociceptin/orphanin FQ release remain unknown. Previous studies in healthy and hypertensive subjects showed that prolonged and forced hyperventilation induces different blood pressure (BP) responses depending on changes in plasma catecholamine levels. We investigated whether the effects of hyperventilation on the sympatho-adrenergic system involve nociceptin/orphanin FQ release. Fifty-six healthy subjects (26 females, mean age 63+/-2 and 30 males, mean age 63+/-3) underwent the hyperventilation test. A hierarchical cluster analysis based on BP response to hyperventilation identified three groups of subjects: group 1 (n=20) with a decrease in BP, norepinephrine (1311.1+/-45.5 fmol/ml versus 900.0+/-55.3 fmol/ml, P<0.01) and nociceptin/orphanin FQ (13.0+/-0.7 pg/ml versus 7.9+/-0.8 pg/ml, P<0.01), group 2 (n=18) without any change in BP and norepinephrine (1133.0+/-31.5 fmol/ml versus 1176.0+/-44.6 fmol/ml), with a decrease in nociceptin/orphanin FQ (12.5+/-3.2 pg/ml versus 7.4+/-0.6 pg/ml, P<0.01) and group 3 (n=18) with an increase in BP, norepinephrine (1216.7+/-50.9 fmol/ml versus 1666.7+/-44.9 fmol/ml, P<0.01) and nociceptin/orphanin FQ values (11.5+/-1.6 pg/ml versus 19.9+/-1.5 pg/ml, P<0.01). Norepinephrine changes in response to hyperventilation in groups 1 and 3 were directly (P<0.01) correlated with those of nociceptin/orphanin FQ. Our results showed that vigorous and prolonged hyperventilation changes plasma nociceptin/orphanin FQ levels due to the direct effects of hypocapnic alkalosis or to different sympatho-adrenergic system responses.
    Peptides 04/2010; 31(4):720-2. · 2.52 Impact Factor
  • Source
    [Show abstract] [Hide abstract]
    ABSTRACT: We investigated the effect of sertraline on inflammation and endothelial function in patients with coronary heart disease (CHD) and symptoms of depression. One hundred patients with CHD and depression were randomized in a double-blind fashion to receive sertraline or a placebo. We measured symptoms of depression (Beck Depression Inventory (BDI) score), levels of inflammatory markers (C-reactive protein (CRP) and interleukin-6 (IL-6)), and flow-dependent endothelium-mediated dilation (FMD) before and after 20 weeks of treatment. Sertraline treatment significantly reduced the BDI score as compared with both baseline and placebo. Levels of CRP and IL-6 also decreased after 20 weeks of sertraline treatment, whereas they did not significantly change in the placebo group. There was a significant improvement in FMD in patients on sertraline treatment, whereas there was no change in FMD in the placebo group. Sertraline improves endothelial function and reduces inflammatory markers in patients with CHD and symptoms of depression.
    Clinical Pharmacology &#38 Therapeutics 07/2009; 86(5):527-32. · 6.85 Impact Factor
  • [Show abstract] [Hide abstract]
    ABSTRACT: The aim of our study was to evaluate the effects of repeated episodes of angina and induced myocardial ischemia on plasma nociceptin/orphanin FQ (N/OFQ) levels. Patients with unstable angina (23 with new onset severe angina or accelerated angina and 18 with subacute angina at rest) who had had repeated spontaneous episodes of chest pain in the last week before the study underwent myocardial perfusion single-photon emission computed tomography using adenosine infusion. Twenty subjects without clinical symptoms of angina matched for age, sex and cardiac risk factors served as a control group. N/OFQ levels were significantly (P<0.01) higher in the patients (15.2+/-2.1 pg/ml) than in the control group (8.5+/-2.6 pg/ml). Blood pressure and heart rate did not significantly differ. All patients showed transient adenosine infusion myocardial ischemia that did not induce chest pain or significantly modify plasma N/OFQ levels or hemodynamic parameters. Our findings show that unstable angina is associated with a significant increase in circulating N/OFQ levels unrelated to intervening transient myocardial ischemia or hemodynamic changes. This increase is probably related to the chest pain repeatedly occurring in the course of coronary artery disease, but absent during transient adenosine-induced myocardial ischemia.
    Peptides 07/2009; 30(9):1705-9. · 2.52 Impact Factor
  • [Show abstract] [Hide abstract]
    ABSTRACT: We evaluated pressor responses to the hyperventilation test in elderly normotensive (n=43, mean age 82 ± 5 years) and elderly hypertensive subjects (n=45 with essential hypertension, mean age 82 ± 2 years, and n=49 with secondary hypertension, mean age 82 ± 3 years). Hyperventilation did not change blood pressure (BP) in normotensive and secondary hypertensive subjects, whereas it decreased BP in essential hypertensives. Hierarchical cluster analysis based on BP responses to hyperventilation disclosed three groups of subjects in each population: group 1 exhibited a reduction in BP (essential hypertensives: 76%), group 2 no change (normotensives: 70%, secondary hypertensives: 76%), and group 3 an increase (normotensives: 19%, essential hypertensives: 13%, secondary hypertensives: 14%). Ambulatory BP monitoring found significant differences in pressor daytime profiles of hypertensive patients according to pressor responses to hyperventilation showing wide fluctuations in group 1 and 3 patients. Interestingly, the peak ambulatory SBP values correlated to the pre-hyperventilation SBP values in group 1, and to the hyperventilation peak SBP values in group 3. In conclusion: 1) Aging decreases reactivity to respiratory alkalosis in elderly normotensives; 2) hyperventilation induces significant pressor changes frequently in essential hypertension, but rarely in secondary hypertension; 3) the significant pressor responses to hyperventilation reflect the daytime pressor profiles predicting the highest daily fluctuations of BP values.
    Central European Journal of Medicine 02/2009; 4(1):17-25. · 0.26 Impact Factor
  • [Show abstract] [Hide abstract]
    ABSTRACT: This study investigated plasma brain natriuretic peptide (BNP) levels in normotensive and hypertensive patients with suspected coronary artery disease during radionuclide pharmacological stress testing. Twenty-seven normotensive patients (15 males, aged 63.0 ± 4.5 years and 12 females, aged 63.0 ± 4.1 years) and 38 essential hypertensive patients (25 males, aged 63.3 ± 3.3 years and 13 females, aged 64.6 ± 2.6 years) with chest pain and exercise stress testing inconclusive for coronary artery disease underwent myocardial perfusion single-photon emission computed tomography (SPECT) using adenosine infusion. SPECT identified patients without (16 normotensive and 22 hypertensive) and patients with (11 normotensive and 16 hypertensive) transient perfusion defects. Basal BNP levels in normotensive patients without transient myocardial ischemia (3.1 ± 1.2 fmol/ml) were significantly (P < 0.01) lower than those observed in normotensive patients with transient ischemia (8.2 ± 1.2 fmol/ml), whereas BNP levels in hypertensive patients without transient ischemia (8.2 ± 1.0 fmol/ml) did not significantly differ from those in hypertensive patients with transient ischemia (8.1 ± 2.0 fmol/ml). No significant difference was found in BNP levels between males or females either in normotensive or hypertensive patients without or with ischemia. Adenosine infusion did not significantly change BNP levels in any subject group without or with myocardial perfusion defects. Our findings show that increases in BNP allow early detection of myocardial ischemia in normotensive patients, but not in hypertensive patients with suspected coronary artery disease. Adenosine-induced myocardial ischemia does not affect BNP production already activated by coronary artery disease in normotensive patients and by hemodynamic changes in hypertensive patients.
    Peptides 01/2009; · 2.52 Impact Factor
  • [Show abstract] [Hide abstract]
    ABSTRACT: It has been observed that a distinct blood pressure (BP) response to prolonged and forced hyperventilation in adult patients with essential hypertension is associated with significant changes in plasma catecholamine and β-endorphin levels. This paper investigated whether hemodynamic and neuro-endocrine responses to hyperventilation in elderly patients with essential hypertension (n = 39, mean age 81 ± 3 years) differ from those in elderly patients with secondary hypertension (isolated systolic hypertension, bilateral chronic nephropathy, nephroangiosclerosis, diabetic nephropathy and hyperparathyroidism) (n = 39, mean age 80 ± 1 years). Plasma β-endorphin levels were normal in patients with essential hypertension and increased in patients with secondary hypertension. Plasma norepinephrine levels were normal in both populations. Hyperventilation decreased BP and norepinephrine levels and increased β-endorphin levels in essential hypertensive patients, whereas it did not significantly change BP or neuro-hormonal levels in secondary hypertensive patients. Hierarchical cluster analysis based on BP response to hyperventilation disclosed a sub-group of essential hypertensive patients with the highest basal levels of norepinephrine and the lowest β-endorphin levels, in whom the BP decrease following hyperventilation was correlated with the decrease in norepinephrine and increase in β-endorphin levels. This suggests that b-endorphin may be involved in modulating sympatho-adrenergic activity in elderly patients with essential hypertension.
    Central European Journal of Medicine 01/2008; 3(1):55-63. · 0.26 Impact Factor
  • [Show abstract] [Hide abstract]
    ABSTRACT: We studied circulating levels of endothelin-1, catecholamines and nitric oxide after a mental arithmetic test in 14 patients with early ischemic lesions of the extremities due to systemic sclerosis and slightly impaired peripheral vascular flow. The test induced an increase (P<0.01) in blood pressure, heart rate, endothelin-1 and catecholamine levels, whereas it did not change the low basal levels of nitric oxide. In healthy subjects (n=20) the test significantly (P<0.01) decreased endothelin-1 without affecting nitric oxide. The low basal levels of nitric oxide and the high plasma concentration of endothelin-1 after psychological stress cannot be explained by an impaired release from the limited ischemic lesions alone. This suggests a diffuse microvascular derangement that aggravates the course of peripheral microvascular ischemic lesions.
    Peptides 12/2005; 26(12):2487-90. · 2.52 Impact Factor
  • Source
    [Show abstract] [Hide abstract]
    ABSTRACT: Cardio-cardiac reflexes may be evoked by both myocardial ischaemia and coronary occlusion itself. The aim of the study was to assess the intrapatient behaviour of autonomic nervous system balance during spontaneous and balloon-induced coronary ischaemia. We studied a group of patients admitted to the coronary care unit for acute coronary syndrome without ST-segment elevation who experienced spontaneous episodes of myocardial ischaemia during bed rest and ECG monitoring. The inclusion criterion was 80-90% lumen stenosis, amenable to angioplasty. Balloon coronary occlusion was performed at 4-6 atmospheres for 120 s. Autonomic nervous system activity was assessed by heart rate variability (HRV) analysis in frequency domain. We analysed 14 episodes of spontaneous ischaemia and 14 episodes of balloon coronary occlusion. During spontaneous ischaemia, HRV showed an increase in the low/high frequencies ratio (11.8 +/- 5.7), as compared to 5 min before and 5 min after (4.4 +/- 2.7 and 3.9 +/- 1.8, respectively) (p = 0.001). The opposite occurred during balloon coronary occlusion (0.8 +/- 0.4 vs. 3.9 +/- 2.0 and 5.1 +/- 2.1, respectively; p = 0.001). Balloon inflation and occlusion evokes baroreceptor vagal predominance in response to a stretch stimulus of the coronary artery. Conversely, spontaneous occlusion during unstable angina is accompanied by naturally occurring sympathetic activation. Sympathetic activation may have a role in the natural history of the disease.
    European Heart Journal 10/2004; 25(17):1502-8. · 14.10 Impact Factor
  • [Show abstract] [Hide abstract]
    ABSTRACT: We studied the effect of pravastatin on coronary perfusion after percutaneous transluminal coronary angioplasty. An exercise test performed within 2 weeks after percutaneous transluminal coronary angioplasty induced reversible perfusion defects in 66% of patients taking pravastatin and 64% of those taking placebo. At follow-up, the exercise test still induced reversible perfusion defects in 3% of patients taking pravastatin and 29% of those taking placebo.
    The American Journal of Cardiology 07/2004; 93(11):1391-3, A6. · 3.21 Impact Factor
  • Source
    [Show abstract] [Hide abstract]
    ABSTRACT: The prognosis for women with chest pain and angiographically normal coronary arteries is believed to be totally benign. Previous studies, however, did not account for the delay of a decade or so in the development of coronary artery disease that women may experience. This study assessed long-term follow-up of 42 women with de novo angina, evidence of reversible myocardial perfusion defects on SPECT, and normal coronary angiograms. At recruitment, all women underwent endothelial function testing (intracoronary acetylcholine) during catheterization. Patients were followed up for >10 years. Angiography was repeated at the end of the follow-up in 37 patients. At recruitment, 22 patients developed diffuse vasoconstriction during acetylcholine in the absence of identifiable focal coronary spasm (acetylcholine-positive group). The remaining 20 patients showed vasodilation (acetylcholine-negative group). At the end of follow-up, in the acetylcholine-positive group, 1 patient developed cardiac death, 13 still complained of chest pain, and 8 had remission of symptoms. In the acetylcholine-negative group, all patients showed complete resolution of chest pain beginning 6 to 36 months after baseline assessment. Angiography showed development of coronary artery disease in the 13 symptomatic patients in the acetylcholine-positive group. In women with angiographically normal-appearing coronary arteries, persistence of chest pain over the years often relates to development of coronary artery disease. Endothelial dysfunction in a setting of normal coronary arteries is a sign of future development of atherosclerosis.
    Circulation 06/2004; 109(21):2518-23. · 15.20 Impact Factor
  • [Show abstract] [Hide abstract]
    ABSTRACT: Twelve patients with chronic critical limb ischemia in whom a spinal cord stimulation (SCS) system had been implanted for at least one year had increased microvascular flow and achieved healing of trophic acral lesions. After switching off the system, the clinical improvement persisted for 10 days and the neurohormonal pattern showed high plasma values of beta-endorphin and Met-enkephalin, normal dynorphin B, endothelin-1 and catecholamines, and low nitric oxide. Met-enkephalin levels were further increased (P < 0.01) immediately after switching on the electrical stimulation again. The persistence of high plasma opioid levels after switching off the spinal cord stimulation explains the absence of subjective complaints and suggests an involvement of opioids in the regulation and improvement of the microcirculation.
    Peptides 04/2004; 25(4):571-5. · 2.52 Impact Factor
  • Source
    [Show abstract] [Hide abstract]
    ABSTRACT: Morbidity of patients with Syndrome X (SX; chest pain and normal coronary angiograms) is high and is associated with continuing episodes of chest pain and hospitalization. Impairment of microvascular endothelial function caused by increased oxidative stress has been suggested to be a mechanism of the disease. Superoxide dismutase (SOD) is the major antioxidant enzyme system of the vascular wall. This study sought to establish whether combination treatment with ACE inhibitors and statins reduces oxidative stress and improves quality of life of patients with cardiac SX. Forty-five patients with SX were randomly assigned to receive either a combination of ramipril (10 mg/d) and atorvastatin (40 mg/d) or placebo for 6 months. We determined the activity of extracellular SOD and its relation to flow-dependent endothelium-mediated dilation (FMD) and quality of life (exercise capacity and score with Seattle Angina Questionnaire [SAQ]) before and after treatment. After 6 months, patients with SX who received atorvastatin and ramipril had significantly reduced (P=0.001) SOD levels (188.1+/-29.6 U/mL). No significant changes were seen on placebo (262.9+/-48.8 U/mL). Reduction of SOD after therapy was negatively correlated with FMD (r=0.38; P=0.01) and positively with total cholesterol (r=-0.56; P<0.001). At follow-up, patients taking atorvastatin and ramipril improved their quality of life both in terms of exercise duration (by 23.46%) and SAQ (by 64.1%). Six months of therapy with atorvastatin and ramipril improves endothelial function and quality of life of patients with SX. Reduced SOD activity may reflect low superoxide anion production. Benefits of these drugs may be related to reduction of oxidative stress.
    Circulation 01/2004; 109(1):53-8. · 15.20 Impact Factor
  • [Show abstract] [Hide abstract]
    ABSTRACT: Previous animal studies suggested that vagal tone contributes to tonic dilatation of coronary arteries. We hypothesized that low parasympathetic activity might be among the causes of coronary instability in the setting of acute coronary syndrome without ST-segment elevation. We studied 172 consecutive patients. Vagal and sympathetic activities were assessed by time domain measures of heart rate variability. PNN50 <3% was used as a marker of low parasympathetic activity. At 6-month follow-up 32 patients developed coronary events. Coronary events were lower during hospitalization (n=9) than during follow-up (n=23). Extremely low values of parasympathetic activity (pNN50 <3%) were strongly related to subsequent events (P<0.001). PNN50 <3% was found in 56% of patients having adverse events versus 5% of patients who had good outcome. Among patients who had pNN50 <3%, 18 patients (72%) had subsequent coronary events vs seven patients (28%) who had a good outcome. These data show that in acute coronary syndrome without ST-segment elevation, a significant number of patients developing subsequent coronary events have a loss of vagal tone. Simple electrocardiographic variables, as pNN50 <3%, may be of great clinical value in identifying patients at high risk of subsequent coronary events even after apparent clinical stabilization.
    European Heart Journal 09/2003; 24(17):1560-6. · 14.10 Impact Factor
  • Source
    [Show abstract] [Hide abstract]
    ABSTRACT: Recent studies show that healthy subjects and patients with moderate hypertension have different pressor responses to hyperventilation, depending on their sympathoadrenergic reactivity. In the present study, we investigated whether a different response to the hyperventilation test is related to differences in the daily blood pressure profiles recorded with noninvasive ambulatory monitoring. Forty-five healthy subjects and 67 patients with essential hypertension of grades 1 and 2 (Joint National Committee VI and World Health Organization) were investigated. Healthy subjects and hypertensive patients responding to hyperventilation with an increase in systolic blood pressure had, during daytime ambulatory blood pressure assessment, peak systolic blood pressure values (146.0+/-5.0 mm Hg, 182.2+/-9.0 mm Hg, respectively) similar to the hyperventilation peak systolic blood pressure values (147.2+/-3.5 mm Hg, 183.0+/-4.7 mm Hg, respectively). Hypertensive patients responding to hyperventilation with a decrease in blood pressure showed clinic systolic blood pressure values (178.4+/-3.2 mm Hg) higher than daytime average ambulatory systolic blood pressure (155.2+/-7.1 mm Hg; P<0.01). Our results indicate that a hyperventilation test yields information on daily peak blood pressure values in healthy subjects and hypertensive patients when it induces a pressor increase and can identify hypertensive patients with the so-called "white coat effect" when it induces a pressor decrease.
    Hypertension 02/2003; 41(2):244-8. · 6.87 Impact Factor
  • [Show abstract] [Hide abstract]
    ABSTRACT: After hyperventilation, systolic and diastolic blood pressure (BP) significantly decreased in 14 hypertensive patients (group 1), did not change in 9 (group 2) and increased in 8 (group 3). Basal BP, norepinephrine and dynorphin B levels were higher in group 1 than in groups 2 and 3. The decrease in BP after hyperventilation was associated with a decrease in plasma norepinephrine, Met-enkephalin and dynorphin B and an increase in beta-endorphin. Naloxone abolished the hyperventilation-induced BP and norepinephrine decreases. Our findings indicate that hyperventilation may select hypertensive patients with different sympatho-adrenergic activity and that the increase in beta-endorphin reduces BP response to hyperventilation in patients with high sympatho-adrenergic tone.
    Peptides 06/2002; 23(5):911-8. · 2.52 Impact Factor
  • [Show abstract] [Hide abstract]
    ABSTRACT: Plasma opioid peptides, norepinephrine, atrial natriuretic factor (ANF) and blood pressure (BP) were assessed in 24 chronic obstructive pulmonary disease patients with acute respiratory failure. Hypoxemic-hypercapnic patients had high BP, beta-endorphin, Met-enkephalin and dynorphin B, whereas hypoxemic-normocapnic and hypoxemic-hypocapnic patients showed normal BP, high beta-endorphin, and normal Met-enkephalin and dynorphin B. Norepinephrine and ANF were high in all patients, particularly in hypoxemic-hypercapnic patients. Infusion with the opioid antagonist naloxone hydrochloride significantly increased systolic blood pressure (SBP) in hypoxemic-hypercapnic (182.0 +/- 3.2 versus 205.1 +/- 3.0 mmHg; P < 0.01), hypoxemic-normocapnic (149.3 +/- 1.8 versus 169.1 +/- 2.2 mmHg; P < 0.01) and hypoxemic-hypocapnic (147.3 +/- 1.3 versus 166.8 +/- 2.2 mmHg; P < 0.01) patients, norepinephrine in hypoxemic-hypercapnic patients (3583.2 +/- 371.8 versus 5371.3 +/- 260.0 fmol/ml; P < 0.01), and reduced ANF in hypoxemic-normocapnic (18.3 +/- 0.8 versus 11.9 +/- 1.0 fmol/ml; P < 0.05) and hypoxemic-hypocapnic (18.1 +/- 1.2 versus 12.1 +/- 2.1 fmol/ml; P < 0.05) patients. These results indicate that the endogenous opioid system attenuates SBP responses in acute respiratory failure by affecting norepinephrine or ANF release.
    Peptides 04/2001; 22(4):631-7. · 2.52 Impact Factor
  • [Show abstract] [Hide abstract]
    ABSTRACT: To investigate the effects of hypoxemia, hypercapnia, and cardiovascular hormones (norepinephrine, endothelin-1, and atrial natriuretic factor) on blood pressure during acute respiratory failure. Patients with chronic obstructive pulmonary disease and acute respiratory failure were divided into four groups of 10 patients each: hypoxemia-normocapnia, hypoxemia-hypercapnia, hypoxemia-hypocapnia, and normoxemia-hypercapnia. Plasma norepinephrine levels were determined by high-performance liquid chromatography with electrochemical detection. Plasma endothelin-1 and atrial natriuretic factor levels were radioimmunoassayed after chromatographic preextraction. Systolic blood pressure and cardiovascular hormone levels were greater in patients with hypercapnia (whether or not they also had hypoxemia) than in those with normocapnia and hypoxemia. For example, in patients with hypercapnia and normoxemia, the mean (+/- SD) systolic blood pressure was 183+/-31 mm Hg and the mean norepinephrine level was 494+/-107 pg/mL, as compared with 150+/- 6 mm Hg and 243+/-58 pg/mL in those with normocapnia and hypoxemia (both P<0.05). Similar results were seen for endothelin-1 and atrial natriuretic factor levels, and for the comparisons of hypoxemic patients who were hypercapnic with those who were normocapnic. These results suggest that blood carbon dioxide levels, rather than oxygen levels, are responsible for hypertension during acute respiratory failure, perhaps as a result of enhanced sympatho-adrenergic activity.
    The American Journal of Medicine 01/2001; 109(8):621-7. · 5.30 Impact Factor
  • [Show abstract] [Hide abstract]
    ABSTRACT: After hyperventilation, systolic blood pressure (SBP) significantly decreased in 10 subjects (group 1), did not change in eight (group 2) and increased in 15 (group 3). Diastolic blood pressure and heart rate increased in all groups. The decrease in SBP was associated with a decrease in plasma catecholamines and increase in beta-endorphin, whereas the increase in SBP was accompanied by an increase in catecholamine and Met-enkephalin levels. Naloxone abolished the hyperventilation-induced SBP and catecholamine decrease only in group 1. These findings show an activation of the endogenous opioid system after hyperventilation and the role of beta-endorphin in reducing SBP in response to the test.
    Peptides 09/2000; 21(8):1223-30. · 2.52 Impact Factor

Publication Stats

524 Citations
195.48 Total Impact Points

Institutions

  • 1986–2010
    • University of Bologna
      • Department of Experimental, Diagnostic and Specialty Medicine DIMES
      Bolonia, Emilia-Romagna, Italy
  • 2004
    • Università degli Studi di Siena
      Siena, Tuscany, Italy
  • 1996
    • Università degli Studi del Sannio
      Benevento, Campania, Italy